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Trace Mineral Deficiencies – Diagnosis and Treatment
Published in Jennifer Doley, Mary J. Marian, Adult Malnutrition, 2023
Kavitha Krishnan, Julianne Werner
Worldwide, about two billion people are iodine-deficient and 2.5% of this population have clinical manifestations of iodine deficiency.50 Iodine deficiency most commonly occurs as a result of consuming a diet insufficient in iodine. The iodine content of plant foods is influenced by the iodine concentration of the soil in which the food is grown. Bread, milk, saltwater fish, and seafood are dietary sources of iodine;51 however, the primary source in many countries is iodized salt.12,52 People who do not consume iodized salt and live in regions with poor soil iodine concentration, as well as those who follow a vegan diet, are at an increased risk of iodine deficiency.51 Consumption of goitrogenic foods, such as soy, cassava, and cruciferous vegetables, also increases the risk for iodine deficiency.53 Use of anti-thyroid medications and other changes in thyroid hormone metabolism can also increase deficiency risk.2,54 For example, iron and selenium deficiency may increase risk as these minerals are necessary for the production of thyroid hormone.55 Pregnant and lactating women may produce anti-thyroid autoantibodies, and have increased glomerular filtration which increases urinary iodine excretion.55
On the Importance of Monitoring Blood Sugar and Other “Vital Signs”
Published in Robert Fried, Richard M. Carlton, Type 2 Diabetes, 2018
Robert Fried, Richard M. Carlton
Thyroid dysfunction was classified as clinical hypothyroidism with TSH greater than 4.20 mUI/mL and FT4 less than 0.93 ng/dL; subclinical hypothyroidism with TSH greater than 4.20 mUI/mL and free T4 less than 0.93 to 1.70 ng/dL. Subclinical hyperthyroidism was considered with TSH less than 0.27 mUI/mL and free T4 was in normal range (0.93 to 1.70 ng/dL), and clinical hyperthyroidism was considered with TSH less than 0.27 mUI/mL and free T4 greater than 1.70 mUI/mL. Autoimmunity was diagnosed with anti-TPO greater than 34 U/mL. Anti-thyroid autoantibodies (anti-TPO) are antibodies targeted against one or more components on the thyroid.
The impact of concurrent Hashimoto thyroiditis on thyroid nodule cytopathology assessed by ultrasound-guided fine-needle aspiration cytology
Published in Postgraduate Medicine, 2020
Fengqiu Hu, Zhe Yan, Buyun Ma, Yong Jiang, Hui Huang
Many factors contribute to an uninformative FNAC outcome. It was recognized that Hürthle cells, which are commonly seen on smears of patients with Hashimoto thyroiditis, and follicular lesions are major difficulties hindering a definitive cytological diagnosis [4,5]. Patients with Hashimoto thyroiditis, clinically characterized by elevated serum anti-thyroid autoantibodies (TgAb and TPOAb) and pathologically characterized by Hürthle cell and diffuse lymphocyte infiltration, are often found with concurrent thyroid nodules (up to 30% of patients) [6,7]. Some studies found that the anti-thyroid autoantibodies were associated with FNAC diagnostic performance, describing a higher incidence of indeterminate FNAC in patients with positive autoantibodies [8]. Therefore, an indeterminate diagnosis has always been the biggest concern in the clinical application of FNAC. For an initial indeterminate FNAC, there are several recommendations, such as repeated FNAC, molecular testing, surveillance or diagnostic surgery. The choice varies depending on clinical evaluation and patient preference. However, if an HT nodule is bound to have a high risk of indeterminate FNAC, then repeated FNAC would hardly help. Whether concurrent HT or increased serum anti-thyroid autoantibodies prevent a thyroid nodule from a conclusive FNAC is uncertain. We hereby conducted this clinical research to analyze the impact of HT on FNAC outcome to provide evidence for the subsequent diagnostic choice when faced with an initial indeterminate FNAC.
The Role of IFN-alpha in Experimental and Clinical Uveitis
Published in Ocular Immunology and Inflammation, 2019
Xiaoli Liu, Maria Diedrichs-Möhring, Gerhild Wildner
Common adverse effects of IFN-α include flu-like symptoms, leukopenia, alopecia, depression, and redness at site of injection. These symptoms are dose dependent and lead to discontinuation of the treatment in some patients.60 Less common are increased liver enzymes, hair loss, fibromyalgia, and worsening of psoriasis (Table 2). Depression was reported in up to 29% of patients, which even led to suicide attempts in some cases.69,70,82,83 Side effects in the 3 Mio U IFN-α2a-treated patients were less frequent and severe.71,72,84,85 Flu-like symptoms were observed in almost all patients treated with IFN-α and mostly disappeared during the first week after initiation of IFN-α. Anti-nuclear (ANA) and anti-thyroid antibodies were detected in some patients; also thyroiditis was induced in a few patients, which might relate to the generation of anti-thyroid autoantibodies.60,69,70 Surprisingly, ocular side effects including Vogt–Koyanagi–Harada and Behçet’s disease, central retinal vein or central retinal artery occlusion and retinopathy, were observed in IFN-α treated hepatitis and leukemia patients, while in IFN-α treated BD patients single cases of retinopathy and non-ischemic optic neuritis were observed.78,85–87
Insulin resistance is associated with larger thyroid volume in adults with type 1 diabetes independently from presence of thyroid autoimmunity
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2018
Anita Rogowicz-Frontczak, Stanislaw Pilacinski, Anna Teresa Chwialkowska, Dariusz Naskret, Dorota Zozulinska-Ziolkiewicz
Thyroid-stimulating hormone (thyrotropin, TSH) level was evaluated in the serum using electrochemiluminescence ECLIA Elecsys analyzers using monoclonal antibodies directed against the human TSH. Normal range was 0.27–4.2 [mIU/L]. Ranges of normal values for adults for free triiodothyronine (FT3) was 3.1–6.8 pmol/L and for free thyroxine (FT4) 12–22 pmol/L. The rating of TSH and free thyroid hormones was performed in patients in a stable metabolic state (glycaemia between 3.89 and 10 mmol/L, absence of ketonuria) [20]. Anti-thyroperoxidase autoantibodies (ATPO) were determined by the ARCHITECT ATPO assay. Results were expressed as international units per litre and the upper level of normal was 5.61 kIU/L. Positive ATPO was defined as ATPO above 5.61 kIU/L. Anti-thyroglobulin antibodies were determined by the ARCHITECT ATg assay. Results were expressed as international units per litre and the upper level of normal was 4.11 kIU/L. Positive ATg was defined as the level of ATg above quantitative in vitro assay 4.0 kIU/L.Anti-TSH receptor antibodies (TRAb) were determined by EUROIMMUN ELISA test. Positive TRAb was defined as TRAb level above 2 kIU/L. Overt hypothyroidism was recognized if TSH was greater than 4.2 [mIU/L] and fT4 levels lower than normal or TSH greater than 10 [mIU/L], subclinical hypothyroidism (SCH) if TSH was between 4.2 and 10 [mIU/L] with free thyroid hormones in the normal range. Subclinical hyperthyroidism was recognized if TSH was less than 0.27 [mIU/L] and free thyroid hormones in the normal range. The diagnosis of autoimmune thyroiditis (AIT) was based on the presence of anti-thyroid autoantibodies ATPO, ATg, TRAb and ultrasonography (hypoechogenicity, parenchymal heterogeneity, lymph nodes) [20].